Cardiac arrest is a significant public health problem cutting across age, race, and gender. A positive impact on cardiac arrest survival has been demonstrated with the substantial reduction in time to defibrillation provided by the widespread deployment of automated external defibrillators (AEDs), and the use of implantable cardioverter defibrillators (ICDs) and implantable pulse generators (IPGs). Examples of AEDs are described in U.S. Pat. Nos. 5,607,454, 5,700,281 and 6,577,102; examples of ICDs are described in U.S. Pat. Nos. 5,391,186, 7,383,085, and 4,407,288, and examples of IPGs are described in U.S. Pat. Nos. 4,463,760, 3,978,865, and 4,301,804, the disclosures of which are incorporated by reference herein.
Optimal resuscitation therapy for out of hospital (OOH) cardiac arrest is the subject of substantial ongoing research. Research has been clear in demonstrating that the timing of resuscitation is of critical importance. For example, there is less than a 10% chance of recovery just ten minutes after the onset of ventricular fibrillation (VF). This knowledge led to the recent widespread deployment of AEDs, primarily in public areas with a high population concentration such as airports and shopping malls. A positive impact on cardiac arrest survival has been demonstrated due to the substantial reduction in time to defibrillation as a result of more available access to AEDs. In addition, for those patients identified as being at particularly high risk, an implantable cardioverter-defibrillator is often implanted in order to address episodes of cardiac arrest without the involvement of a rescuer.
In the case of VF, performing CPR-type chest compressions before defibrillation or between successive defibrillation shocks and minimizing the time to defibrillation shock following the cessation of the CPR chest compressions is important in facilitating effective recovery especially in cases of long duration VF. It is generally believed that perfusion of the myocardium achieved during CPR preconditions the heart for the defibrillating shock. Despite the importance of CPR, it is often not performed in the field for a variety of reasons.
MVT has also been recognized as a way of forcing some amount of cardiac output by electrically stimulating muscle tissue directly with stimuli that cause the heart or skeletal muscles to contract in a controlled cycle. See U.S. Pat. Nos. 5,735,876, 5,782,883 and 5,871,510. These patents describe implantable devices having combined defibrillation, and MVT capability for forcing cardiac output. U.S. Pat. No. 6,314,319 describes internal and external systems and associated methods of utilizing MVT to achieve a hemodynamic effect in the heart as part of an implantable cardioverter defibrillator (ICD) for purposes of achieving a smaller prophylactic device. The approach described in the '319 patent uses the MVT therapy to provide a smaller and less expensive implantable device that can maintain some cardiac output without necessarily providing defibrillation therapy.
Unlike a conventional defibrillator, which operates with the primary purpose of restoring a normal cardiac rhythm, or an IPG that operates to control the rate of an existing cardiac rhythm, MVT stimulation can be used to provide cardiac output, which in turn causes perfusion to the heart and brain, as well as other critical body tissues. By providing perfusion to the heart and other vital organs, MVT prolongs the life of the patient even while the patient continues experiencing the arrhythmia. Additionally, MVT improves the likelihood of successful defibrillation or of a spontaneous return of circulation. An AED equipped with MVT can provide consistent high quality chest compressions. In the case of an implanted ICD or IPG, back up chest compressions provided by MVT can, in one sense, be even more important than in an external, since in the case of the implantable device there may be no rescuer available to perform CPR when needed.
U.S. Patent Application Publication No. 2006/0142809, the disclosure of which is incorporated by reference herein, describes a technique and associated apparatus that combines defibrillation therapy with MVT into an external device having a capability to perform electrical CPR. Externally-applied MVT is proposed for stimulating skeletal and sympathetic muscles in addition to myocardial muscle tissue to effect chest compression and even ventilation in the patient. The '809 publication reflects the knowledge in the art that due to the inclusion of differing time constant components in an MVT waveform, the waveform can stimulate contraction of a variety of different types of muscles, e.g., myocardial, skeletal, sympathetic muscles, and the phrenic nerve. Varying and controlling the MVT waveform parameters, including variation of the musculature targeted by the waveform, is described as a way to maximize coronary perfusion pressure generated by application of MVT.
Separately, there have been developments in automated chest compression devices that apply mechanical pressure in repeated CPR-like cycles to a patient's chest area. These devices may incorporate defibrillation therapy as well, such as disclosed in U.S. Pat. No. 6,398,744. Although mechanical chest compression devices are useful in situations where sustained manual CPR is difficult or tiring for rescuers, such as in lengthy ambulance trips or airlifts, for example, these devices include a belt that must be positioned around a patient's chest, making them generally unsuitable for use by layperson rescuers. There is also no implantable analogous device that could apply mechanical chest compressions.
More recently, a mechanical chest compression device has been used to study the effects of delivering defibrillation therapy at various points in the chest compression cycle. U.S. Pub. No. 2009/0149903 discloses the results of animal research in which the mechanical chest compression cycle of a porcine model was measured directly using a load cell force transducer, the output of which was used to control the time of application of the defibrillation energy. The empirical results of this work suggest that application of the defibrillation therapy at the end upstroke phase of the compression cycle produced an increased success rate of converting the ventricular fibrillation.
It would be desirable to apply some of these chest compression cycle-defibrillation synchronization principles learned from mechanical chest compression technology to devices utilizing MVT to take advantage of the ease of use of AED devices requiring only the placement of electrodes, plus the ability to implement compression cycle-defibrillation synchronization in implantable devices. Previously, it has been proposed to time a defibrillation shock after a skeletal muscle stimulating pre-shock waveform for an implanted subcutaneous device, as disclosed in U.S. Pub. No. 2004/00220628. This approach attempts to compress the thorax to reduce conduction path length for the subsequent defibrillation shock, thereby reducing the defibrillation shock impedance and concentrating the defibrillation current to the heart.
Synchronizing electrically-stimulated chest or heart compressions with defibrillation therapy presents its own set of challenges. Although the defibrillation pulses can be precisely timed relative to the start or cessation of the muscle stimulation by triggering the discharge of appropriate waveforms and energy at the appropriate times, synchronizing the defibrillation pulses to the chest compressions themselves is not so straight-forward to control. For instance, each individual patient has a particular size, chest cavity structure, lung volume, skeletal muscle mass, muscle tone, heart volume and mass, etc. These all factor into the characteristics of the compression cycle that can be produced by applying MVT, and vary patient-to-patient. Likewise, the particular patient's disease state or symptoms thereof, such as cardiomegaly, i.e., enlarged heart, for example, can affect the timing and quality of the compression cycle induced by MVT administration. Moreover, electrical muscle stimulation approaches cannot directly measure the compression cycle using the type of load cell sensor disclosed in the 2009/0149903 publication.
The 2004/00220628 publication recognizes some of these challenges and proposes that the time delay between the pre-shock waveform and the defibrillation shock be varied patient-to-patient or shock-to-shock. However, this reference does not address how the time delay is to be varied, or what the basis for varying the time delay should be. Moreover, it is not apparent from the art whether the seemingly contradictory teachings of the 2004/00220628 publication emphasizing applying the defibrillation shock at the point where the chest is most compressed, can be reconciled with the findings of U.S. Pub. No, 2009/014990 suggesting the optimal point of defibrillation shock delivery should be when the chest has rebounded after a chest compression.
Optimal arrhythmia treatment continues to be a subject of ongoing research and development. In spite of the substantial progress in the research to understand the underlying biological mechanisms in electrical conversion of arrhythmias, a complete understanding (beyond here hypotheses) of the effects of all of the associated parameters, such as the effect of chest compressions, has been elusive. There remains a need for further improvement of treatment apparatus and associated processes to increase the effectiveness of these life-saving therapies.